αFAP-specific nanobodies mediate a highly precise retargeting of modified AAV2 capsids thereby enabling specific transduction of tumor tissues.

Due to the refractiveness of tumor tissues to adeno-associated virus (AAV) transduction, AAV vectors are poorly explored for cancer therapy delivery. Here, we aimed to engineer AAVs to target tumors by enabling the specific engagement of fibroblast activation protein (FAP). FAP is a cell surface receptor distinctly upregulated in the reactive tumor stroma, but rarely expressed in healthy tissues.

Pharmacological and pre-clinical safety profile of rSIV.F/HN, a hybrid lentiviral vector for cystic fibrosis gene therapy.

Rationale And Objective: Cystic fibrosis (CF) is caused by mutations in the CF Transmembrane Conductance Regulator (CFTR) gene. CFTR modulators offer significant improvements, but approximately 10% of patients remain nonresponsive or are intolerant. This study provides an analysis of rSIV.

Ineffective responses to unlikely outbreaks: Hypothesis building in newly-emerging infectious disease outbreaks.

Over the last 30 years, there has been significant investment in research and infrastructure aimed at mitigating the threat of newly emerging infectious diseases (NEID). Core epidemiological processes, such as outbreak investigations, however, have received little attention and have proceeded largely unchecked and unimproved. Using ethnographic material from an investigation into a cryptic encephalitis outbreak in the Brong-Ahafo Region of Ghana in 2010-2013, in this paper we trace processes of hypothesis building and their relationship to the organizational structures of the response.

Combining SOS1 and MEK Inhibitors in a Murine Model of Plexiform Neurofibroma Results in Tumor Shrinkage.

Individuals with neurofibromatosis type 1 develop rat sarcoma virus (RAS)-mitogen-activated protein kinase-mitogen-activated and extracellular signal-regulated kinase (RAS-MAPK-MEK)-driven nerve tumors called neurofibromas. Although MEK inhibitors transiently reduce volumes of most plexiform neurofibromas in mouse models and in neurofibromatosis type 1 (NF1) patients, therapies that increase the efficacy of MEK inhibitors are needed. BI-3406 is a small molecule that prevents Son of Sevenless (SOS)1 interaction with Kirsten rat sarcoma viral oncoprotein (KRAS)-GDP, interfering with the RAS-MAPK cascade upstream of MEK.

Targeting motifs in frustule-associated proteins from the centric diatom .

The frustule of diatoms has an exceptional structure composed of inorganic and organic molecules. In the organic fraction, protein families were identified whose members are expected to have a complex cellular targeting to their final location within the frustule. Here we investigated for frustule-targeting signals two representatives of the cingulin family, the proteins CinY2 and CinW2; beside an already known, classical signal peptide, we have identified further regions involved in cellular targeting.